Dr. Chan has over 25 years of experience as an orthopedic surgeon, inventor, researcher and entrepreneur. He has brought a number of innovations from concept to the standard of surgical care, including a vacuum mixing system for total joint replacements and a suture passer for arthroscopic surgery. He is currently an Adjunct Professor at the National University of Singapore (NUS), with appointments at the Department of Orthopaedic Surgery and the Division of Bioengineering, a Fellow of the American Academy of Orthopedic Surgeons and a Fellow of the Canadian Academy of Sport Medicine. His previous experience as the Director of Technology Transfer Office and as the Senior Director of NUS Enterprise at the National University of Singapore provide Dr. Chan with unique executive and management skills. He is currently on the governing board of the Mechanobiology Research Center of Excellence, Singapore. He teaches a course on Bioengineering Design for the third-year Bioengineering students at NUS. He holds a Master’s Degree of Applied Science in Aerospace Engineering from the University of Toronto, a Doctor of Medicine degree from the University of Toronto, completed orthopedic surgery training at the University of Toronto Residency Program and completed a spine fellowship under Dr Ian MacNab. His research interests lie in the area of tissue engineering and the effects of nanotexture on stem cell differentiations. He has been published in over 50 peer-reviewed publications and he currently holds 39 issued U.S. patents, with more patents pending.
Google Scholar Profile at http://goo.gl/r9GsC

Linking beta -catenin to androgen-signaling pathway.

ABSTRACTThe androgen-signaling pathway is important for the growth and progression of prostate cancer cells. The growth-promoting effects of androgen on prostate cells are mediated mostly through the androgen receptor (AR). There is increasing evidence that transcription activation by AR is mediated through interaction with other cofactors. beta-Catenin plays a critical role in embryonic development and tumorigenesis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction. Here, we demonstrate that a specific protein-protein interaction occurs between beta-catenin and AR. Unlike the steroid hormone receptor coactivator 1 (SRC1), beta-catenin showed a strong interaction with AR but not with other steroid hormone receptors such as estrogen receptor alpha, progesterone receptor beta, and glucocorticoid receptor. The ligand binding domain of AR and the NH(2) terminus combined with the first six armadillo repeats of beta-catenin were shown to be necessary for the interaction. Through this specific interaction, beta-catenin augments the ligand-dependent activity of AR in prostate cancer cells. Moreover, expression of E-cadherin in E-cadherin-negative prostate cancer cells results in redistribution of the cytoplasmic beta-catenin to the cell membrane and reduction of AR-mediated transcription. These data suggest that loss of E-cadherin can elevate the cellular levels of beta-catenin in prostate cancer cells, which may directly contribute to invasiveness and a more malignant tumor phenotype by augmenting AR activity during prostate cancer progression.